Antral-type mucosa in the gastric incisura, body, and fundus (antralization): a link between Helicobacter pylori infection and intestinal metaplasia?

OBJECTIVES: Helicobacter pylori is a carcinogen; gastric carcinoma involves a multistep process from chronic gastritis to atrophy, intestinal metaplasia, and dysplasia. The aims of this study were to determine the types of mucosa at different gastric sites in H. pylori-infected and uninfected patients, and whether the presence of antral-type mucosa in the incisura, body, and fundus is associated with gastric atrophy and intestinal metaplasia. METHODS: Two hundred and sixty-eight patients with dyspepsia were enrolled. Eight biopsies (i.e., antrum x3, body x2, fundus x2, and incisura x1) were obtained. One antral biopsy was used for the CLO-test. Three (each from the antrum, body, and fundus) were cultured. The remaining biopsies were examined histologically according to the updated Sydney System after staining with hematoxylin and eosin and Giemsa. A validated serological test was also applied. RESULTS: Overall, 113 (42%) patients were infected with H. pylori. At the incisura, antral-type mucosa was more prevalent in infected than in uninfected patients (84% vs. 18%; odds ratio [OR] = 23.9, 95% confidence interval [CI] 12.5-45.8; p<0.001). Atrophic gastritis and intestinal metaplasia at the incisura was present in 19.5% and 13.3%, respectively, of infected, and 4.5% and 3.2%, respectively, of uninfected patients (both p<0.01). Moreover, atrophic gastritis at the incisura was associated with the presence of antral-type mucosa at the site (termed antralization); the prevalence of atrophic gastritis was 19.5% (24/123) in the presence of antralization, whereas the rate was 2.1% (3/145) without antralization (OR = 11.4, 95% CI 3.4-39.2; p<0.001). Similarly, at the incisura, 16.3% (20/123) of "antralized" cases and 1.4% (2/145) of "unantralized" cases had intestinal metaplasia (OR = 13.8, 95% CI, 3.2-60.7; p<0.001). The association between antralization at gastric body and fundus also appeared to be associated with atrophic gastritis and intestinal metaplasia at these sites. CONCLUSIONS: Atrophic gastritis and intestinal metaplasia occurs predominantly at the gastric antrum and incisura with H. pylori infection. Antralization of the gastric incisura is a common event in H. pylori-infected patients, and appears to be associated with an increased risk of atrophic gastritis and intestinal metaplasia.     

Association of Helicobacter pylori infection with atrophic gastritis and intestinal metaplasia

AIMS: To evaluate the effect of Helicobacter pylori infection and aging on atrophy and intestinal metaplasia of the gastric mucosa. METHODS: One hundred and sixty-three patients were divided into three age groups and underwent an upper gastrointestinal endoscopy where no esophagitis, peptic ulcers, or malignancies were detected. Two biopsy specimens were obtained from the anterior and posterior walls of the antrum and of the fundus. These were used to evaluate the grade of gastritis, bacterial culture and histologic evidence of H. pylori infection. RESULTS: Helicobacter pylori infection was found to be directly associated with an increased risk of gastritis grade (odds ratio (OR) = 90 (95% CI; 30-270)). An age of 60 years and older along with H. pylori infection was also strongly associated with an increased risk of atrophy (OR = 6.6, (95% CI; 2.9-15.2)); OR = 9.8, (95% CI; 2.7-35.4)), as was intestinal metaplasia of the gastric mucosa (OR = 5.5, (95% CI; 1.7-17.6)); OR = 7.9, (95% CI; 2.8-46.1)). The prevalence of atrophic gastritis increased with advancing age in H. pylori-infected patients, but no such phenomenon was observed in H. pylori-uninfected patients. The prevalence of intestinal metaplasia significantly increased with advancing age, irrespective of the presence of H. pylori infection. In addition, H. pylori uninfected female patients had a decreased risk of intestinal metaplasia. CONCLUSIONS: These results suggest that atrophic gastritis is not a normal aging process, but instead is likely to be the result of H. pylori infection, while intestinal metaplasia is caused by both the aging process and H. pylori infection. A decreased risk of intestinal metaplasia found in uninfected female subjects may partly explain the lower prevalence of gastric cancer in females than in males.     

胃黏膜病变演化过程中抗氧化蛋白Peroxiredoxin6的表达及其与幽门螺杆菌感染的关系

目的探讨胃黏膜病变演化过程中抗氧化蛋白Peroxiredoxin 6(Prx6)表达水平变化及其与幽门螺杆菌(H.pylori)感染的关系。方法根据组织形态学将104例临床内镜检查活检标本分为慢性浅表性胃炎(33例)、慢性萎缩性胃炎(25例)、肠上皮化生(32例)及异型增生(14例)4组。用免疫组织化学方法检测组织标本中Prx6的表达水平。用快速尿素酶试验及Warthin-Starry银染检测H.pylori感染。结果 Prx6在慢性浅表性胃炎、慢性萎缩性胃炎、肠上皮化生、异型增生组的阳性表达率分别为39.4%(13/33)、80.0%(20/25)、93.8%(30/32)、92.9%(13/14),过表达率分别为15.2%(5/33)、44.0%(11/25)、81.3%(26/32)、85.7%(12/14)。慢性浅表性胃炎、慢性萎缩性胃炎组H.pylori阳性者Prx6阳性表达率显著高于H.pylori阴性者(P<0.05),肠上皮化生组Prx6的表达在H.pylori阳性者和阴性者无显著差异(P>0.05)。结论在胃黏膜病变演化过程中,Prx6的表达随着胃黏膜病变的进展而增加,H.pylori在胃黏膜病变演化的早期阶段促进了Prx6的表达。     

Coordinate increase of telomerase activity and c-Myc expression in Helicobacter pylori-associated gastric diseases

AIM: To detect the telomerase activity and c-Myc expression in gastric diseases and to examine the relation between these values and Helicobacter pylori (H pylori) as a risk factor for gastric cancer. METHODS: One hundred and seventy-one gastric samples were studied to detect telomerase activity using a telomerase polymerase chain reaction enzyme linked immunosorbent assay (PCR-ELISA), and c-Myc expression using immunohistochemistry. RESULTS: The telomerase activity and c-Myc expression were higher in cancers (87.69% and 61.54%) than in noncancerous tissues. They were higher in chronic atrophic gastritis with severe intestinal metaplasia (52.38% and 47.62%) than in chronic atrophic gastritis with mild intestinal metaplasia (13.33% and 16.67%). In chronic atrophic gastritis with severe intestinal metaplasia, the telomerase activity and c-Myc expression were higher in cases with H pylori infection (67.86% and 67.86%) than in those without infection (21.43% and 7.14%). c-Myc expression was higher in gastric cancer with H pylori infection (77.27%) than in that without infection (28.57%). The telomerase activity and c-Myc expression were coordinately up-regulated in H pylori infected gastric cancer and chronic atrophic gastritis with severe intestinal metaplasia. CONCLUSION: H pylori infection may influence both telomerase activity and c-Myc expression in gastric diseases, especially in chronic atrophic gastritis.     

Helicobacter pylori-associated gastritis and gastric cancer in Nigeria.

BACKGROUND: The etiology of gastric cancer has not been clearly delineated. There is some evidence of an association of gastric cancer with Helicobacter pylori-induced chronic gastritis, atrophic gastritis and intestinal metaplasia. Previous studies report a high rate of H. pylori infection and chronic gastritis among Nigerians. METHODS: We retrospectively reviewed 84 tissue specimens with gastric cancer seen in our department over an 18-year period for for the presence of H. pylori infection, chronic gastritis, atrophic gastritis, and intestinal metaplasia in the adjacent non-cancerous gastric mucosa. RESULTS: H. pylori infection was detected in 15 (17.9%) of 84 specimens. Moderate to severe gastritis was found in non-cancerous areas in 77 (91.7%) specimens, and was equally frequent in patients with 'intestinal' and 'diffuse' types of cancer. Atrophic gastritis and intestinal metaplasia were observed in 22 (26.2%) and 35 (41.7%) specimens, respectively, and were more common in 'intestinal' type of gastric cancer. CONCLUSION: Chronic gastritis was seen in the adjacent non-cancerous mucosa in most specimens with gastric cancer. However, its severity did not correlate with the histological subtype of gastric cancer.     

Gastric epithelial cell kinetics in the progression from normal mucosa to gastric carcinoma.

Increased epithelial cell proliferation is associated with an increased risk of adenocarcinoma and is associated with Helicobacter pylori infection. The aim of this study was to assess both gastric epithelial cell proliferation and the influence of H pylori infection on cell kinetics in the progression from normal mucosa to gastric carcinoma. One hundred and forty four subjects were assigned to study groups based on diagnosis and H pylori status: microscopically normal mucosa and H pylori negative (n = 28); chronic active gastritis and H pylori positive (n = 83); atrophic gastritis (n = 9); intestinal metaplasia (n = 19); gastric carcinoma (n = 12). Gastric antral epithelial cell proliferation was assessed using the in vitro bromodeoxyuridine immunohistochemical technique and expressed as the labelling index per cent (LI%). Subjects with chronic atrophic gastritis, intestinal metaplasia or gastric cancer have increased gastric epithelial cell proliferation compared with normal mucosa (LI% mean (SEM): 5.14 (0.6), 4.68 (0.3), 6.50 (0.5) v 3.08 (0.2), p < 0.001). This increase in gastric epithelial cell proliferation was not influenced by H pylori status. Gastritis associated with H pylori had an increased LI% compared with normal controls or subjects with H pylori negative gastritis (4.98 (0.2) v 3.08 (0.2), 3.83 (0.2), p < 0.01). H pylori infection although associated with an increased epithelial cell proliferation in subjects with chronic gastritis, does not influence the increased epithelial cell proliferation seen in subjects with precancerous lesions or gastric carcinoma. This is further evidence that H pylori may be an initiating step in gastric carcinogenesis.     

幽门螺杆菌感染者胃粘膜癌前病变与Fas抗原表达的关系

目的研究幽门螺杆菌(Hp)感染后胃粘膜癌前病变中 Fas 抗原表达的情况,了解 Hp 在胃癌发生过程中的作用。方法采用免疫组织化学等方法检测83例经病理证实为慢性胃炎病人胃粘膜上皮细胞中 Fas 抗原的表达情况。结果在浅表性胃炎、萎缩性胃炎、肠化生及异型增生中,Fas 抗原表达率分别为20.00%、36.36%、73.33%、43.75%,Fas 抗原在肠化生中的表达率显著高于浅表性胃炎、萎缩性胃炎及异型增生(P<0.01及P<0.05)。Hp 感染者 Fas 抗原表达率为60.71%,显著高于 Hp 阴性者的22.22%(P<0.01)。在萎缩、肠化生及异型增生等癌前病变中,Hp 感染者与未感染者表达率分别为65.96%及28.57%(P<0.01)。结论 Hp 感染对 Fas 抗原表达有一定的影响,Hp 感染可促进 Fas 抗原表达增加,这可能是 Hp 感染诱导胃粘膜上皮细胞凋亡的机制之一。     

Prevention by bovine milk against Helicobacter pylori-associated atrophic gastritis through its adherence inhibition

BACKGROUND/AIMS: The effects of Helicobacter pylori infection on the development of atrophic gastritis and intestinal metaplasia in relation to lifestyle and diet and the effect of the bovine milk on H. pylori adherence to gastric antral mucosa were investigated. METHODOLOGY: H. pylori infection was investigated in 63 patients without endoscopic evidence of gastroduodenal disease. Presence of H. pylori infection was assessed by culture and histologic examination of antral and corpus biopsy samples. Grades of atrophic gastritis and intestinal metaplasia were judged with chromoendoscopy (Congo red-methylene blue test). Adherence of H. pylori was evaluated with scanning electron microscopic examination of antral mucosa in Mongolian gerbils. RESULTS: Cross-sectional analysis of lifestyle and diet showed that a high intake of bovine milk was significantly related to prevention of H. pylori infection and the developments of atrophic gastritis and intestinal metaplasia. H. pylori adherence to the gastric mucosa was inhibited by bovine milk in a dose-dependent manner. CONCLUSIONS: Bovine milk prevents the development of atrophic gastritis and intestinal metaplasia through its defense mechanisms against the attachment of H. pylori to the gastric mucosa.     

慢性胃炎胃黏膜细胞DNA含量和增殖活性的流式细胞仪检测

背景慢性萎缩性胃炎是一种胃癌癌前状态,研究表明正常胃黏膜、癌前病变和胃癌细胞的DNA含量随病变的进展而逐渐增高。目的应用流式细胞仪检测慢性胃炎胃黏膜细胞的DNA含量和增殖活性,探讨两者在慢性胃炎发生、发展过程中的临床意义。方法选取90例经胃镜检查诊断为慢性胃炎者的胃黏膜活检标本,制备单细胞悬液,应用流式细胞仪进行细胞DNA含量和增殖活性检测。结果所有慢性胃炎胃黏膜细胞的DNA倍体类型均为二倍体,但慢性萎缩性胃炎和慢性萎缩性胃炎伴肠化生胃黏膜细胞的增殖指数(PI)较慢性非萎缩性胃炎显著增高(P<0.05)。除慢性非萎缩性胃炎外,其余慢性胃炎组幽门螺杆菌(H.pylori)阳性患者胃黏膜细胞的PI值均较阴性患者显著增高(P<0.05)。结论慢性萎缩性胃炎和H.pylori阳性慢性胃炎胃黏膜细胞的增殖活性显著增高。应用流式细胞仪检测胃黏膜细胞的DNA含量和增殖活性,也许能成为胃癌癌前状态和癌前病变病理诊断的参考指标。     

幽门螺杆菌相关性胃炎和胃癌前期病变的发病机制

幽门螺杆菌（H．pylori）感染诱发胃黏膜的炎症反应是引起一切病变的基础，并且它在慢性胃炎→萎缩性胃炎→胃黏膜肠上皮化生→不典型增生→胃癌的演变过程中至始至终起作用，因此H．priori相关性胃炎是H．priori致病的启动因子。H．priori感染可引起胃黏膜局部固有和获得性免疫异常，炎症介质的释放、ROS和NO含量的异常，胃上皮细胞增殖与凋亡失衡，端粒酶及相关基因表达异常。这些因素综合作用引起胃黏膜炎症，并且由其发展为胃癌前病变，最终导致胃癌发生。     

Helicobacter pylori and gastric premalignant conditions.

A hypothetical sequence occurs in the stomach from H. pylori infection to premalignant conditions. This sequence is characterized by several well documented steps. First, the H. pylori infection seems to be the main course of chronic gastritis, and is seen to be associated with gastritis at least in 80% of the cases. Second, chronic gastritis tends to slowly progress to atrophy and intestinal metaplasia of the underlying mucosa in a great proportion of affected subjects, this progression of chronic gastritis to atrophy being, however, multifactorial in nature, and being obviously affected also by factors other than the H. pylori. Third, there occurs an increased risk of gastric cancer in atrophic stomach (atrophic gastritis) with intestinal metaplasia, this risk being dependent upon the extend and grade of atrophic and metaplastic alterations in the stomach. Thus, it can be suggested that the H. pylori infection may trigger a sequence which will finally result in a development of conditions that favour the cancer formation. Recent epidemiological observations support this view: gastric cancer tends to be common in populations in which the H. pylori infection and the gastritis are common and in which the people will be commonly infected already in childhood, or in young age.     

Helicobacter pylori infection and precancerous lesions of the stomach

H. pylori infection is associated with a slightly increased risk of gastric cancer. However, the risk is much higher in the subgroup of infected patients who have atrophic gastritis and extensive intestinal metaplasia. In those subjects, H. pylori acts as a trigger of the sequence which begins as atrophic gastritis with intestinal metaplasia and evolves towards immature forms of intestinal metaplasia and dysplasia. It seems that factors different from H. pylori (diet, genetical background, etc.) might have an influence on how often gastric precancerous lesions appear in H. pylori-infected subjects. Effective prevention of gastric carcinoma would require identification of the patients at risk in an early step of the process. Preventive measures would include H. pylori eradication and changes in the diet (i.e., increase of vitamin C and carotenoid intake). Preliminary data suggest that H. pylori eradication cannot revert intestinal metaplasia. However, it is possible that eradication of the bacteria would prevent progression towards immature forms of intestinal metaplasia and dysplasia.     

Diagnosis of Helicobacter pylori infection in patients with atrophic gastritis: comparison of histology, 13C-urea breath test, and serology

BACKGROUND: Atrophic gastritis, a risk factor for gastric cancer, is a late consequence of Helicobacter pylori infection in approximately one-third of the infected patients. It has been suggested that gastric cancer would develop less frequently if H. pylori were eradicated. However, the prevalence of H. pylori infection may be underestimated in patients with atrophic gastritis and intestinal metaplasia if only biopsy-based diagnostic methods are used. METHODS: We compared histology, 13C-urea breath test (13C-UBT), and serology in H. pylori diagnostics in 50 male patients with atrophic corpus gastritis. RESULTS: H. pylori was detected in 15 (30%) patients by histology and in 14 (28%) by 13C-UBT, whereas increased serum antibody levels indicating H. pylori infection were found in 41 (82%) patients (P < 0.0001 between serology and both histology and 13C-UBT). H. pylori infection was associated with atrophic corpus gastritis in 84% of the present patients (in one patient with normal antibody titres H. pylori was defined histologically). CONCLUSIONS: H. pylori infection would have been missed in most patients with atrophic gastritis without the analysis of H. pylori antibodies. Therefore, in patients with atrophic gastritis, the use of serology is encouraged in diagnosing H. pylori infection.     

Expression of gastric cancer—associated MG7 antigen in gastric cancer,precancerous lesions and H.pylori—associated gastric diseases

AIM: To investigate the relationship between the antigen MG7 antigen expression and gastric cancer as well as precancerous condition; to study the relationship between the MG7 antigen expression and H. pyloriinfection in benign gastric lesions in order to find out the effect of H. pylori infection on the process of gastric cancer development.METHODS: The level of MG7 antigen expression was determined by immunohistochemical method in 383 gastric biopsied materials. The intestinal metaplasia was determined by histochemistry method. The H. pyloriinfection was determined by HE stain, PCR and ELISA in 291 specimens, among which only 34 cases of H. pylori-associated gastric lesions were followed up.RESULTS: The positive rate of MG7 expression in normal gastric mucosa, intestinal metaplasia, dysplasia and gastric cancer increased gradually in ascending order (P＜0.01). The positive rate of MG7 antigen expression in type Ⅲ intestinal metaplasia of gastric mucosa was higher than that of type Ⅰand Ⅱ intestinal metaplasia, being highly significant (P＜0.05).The positive rate of MG7 antigen expression in superficial gastritis, atrophic gastritis and gastric cancer increased gradually (11.9 %, 64.8 %, 91.2 %, P＜0.01). There was no significant difference between H.pylori-negative and H. pyloripositive intestinal metaplasia, atrophic gastritis and dysplasia of gastric epithelium in the positive rate of MG7 antigen expression. There was no expression of MG7 antigen in H. pylori-negative superficial gastritis. The positive rate of MG7 expression in H. pylori-positive superficial gastritis was 20.5 %, and the difference between them was significant (P＜0.05). During following up, one of the three H. pylori negative cases turned positive again, and its MG7 antigen expression turned to be stronger correspondingly. 3 of 31 H. pyloripositive cases were detected as early gastric cancer, among which one with "+++" MG7 antigen expression was diminished after H. pylori eradication.CONCLUSION: MG7 antigen expression is highly specific in gastric cancer and can be used as a good marker for screening of gastric cancer; type Ⅲ intestinal metaplasia, atrophic gastritis and dysplasia should be followed up and MG7 antigen expression has high clinical value in the dynamic follow-up study; although the positive -MG7 in positiveH. pylorisuperficial gastritis show benign morphology in features, there is still the potential risk of developing into gastric cancer, hence special attention should be paid to those showing increasing MG7 antigen expression.     

胃黏膜癌前病变中p53、p21^ras蛋白表达与幽门螺杆菌感染的关系

目的观察幽门螺杆菌(Helicobacterpylori)感染及根除H.pylori二年后p53、p21ras在二组胃黏膜上皮细胞的表达,探讨H.pylori在胃癌发生、发展中的作用.方法应用免疫组织化学染色、尿素酶快速试验(RUT)、组织学Warthin-Starry染色.198例H.pylori感染患者,慢性胃炎86例,慢性胃炎伴肠化生67例,慢性胃炎伴异型增生45例;对照组为根除H.pylori 2年后共86例,其中慢性胃炎54例,慢性胃炎伴肠化生32例,慢性胃炎伴异型增生10例.全部病例做p53、p21ras免疫组织化学染色.结果 H.pylori感染组p53、p21 ras 阳性表达率15.7%、18.7%,明显高于H.pylori根除组2.3%、7%,差异显著(P＜0.05);慢性胃炎伴肠化病变中,p53、p21ras在H.pylori感染组阳性表达率17.9%、18.4%均高于H.pylori根除组0%、9.4%,差异显著(P＜0.05)慢性胃炎伴异型增生病变中,p53、p21 ras在H.pylori感染组阳性表达率31.1%、40%均高于H.pylori根除组20%、30.4%,差异显著(P＜0.05);H.pylori 感染组p53、p21ras在慢性胃炎,肠化生,异型增生表达水平依次增高p53、p21ras共同表达阳性37例.结论在胃黏膜癌前病变中p53、p21ras 在H.pylori感染组阳性表达率高于H.pylori根除组,差异显著(P＜0.05);在慢性胃炎,肠化生,异型增生p53、p21ras表达水平在增高;p53、p21 ras表达呈正相关;H.pylori感染在胃癌发生、发展过程中起一定作用,p53、p21ras表达可能是H.pylori致癌的作用机理之一.     

胃粘膜癌前病变中幽门螺杆菌与c-met原癌基因蛋白表达关系的研究

为研究Hp感染后胃粘膜细胞中c-met原癌基因蛋白表达的情况,了解Hp在胃癌发生过程中的作用,对110例经病理证实为慢性胃炎的病人用免疫组化方法检测了胃粘膜细胞中e-met原癌基因蛋白表达情况。结果表明,在浅表性胃炎、萎缩性胃炎、肠化生及异型增生中,e-met原癌基因蛋白的表达率分别为22.2％、44.1％、67.5％和61.9％。过表达率分别为5.5％、26.4％、37.8％和38.1％。Hp感染后c-met原癌基因蛋白表达率较末感染者高,分别为63％及32％,在萎缩,肠化生及异型增生等癌前病变中Hp感染者与未感染者表达率分别为58.9％及29.7％(P<0.005)。本研究结果显示,随着病变的进展,c-met原癌基因的表达随之增加,从而说明Hp感染对c-met原癌基因蛋白表达有一定的影响,Hp启动了胃癌发展的早期阶段,也可能推进胃癌的发展过程。     

Pathogenic implications of interleukin-8 activity and bacterial phenotype in antral gastritis associated with Helicobacter pylori.

OBJECTIVE: Helicobacter pylori (Hp) infection is characterized by an intense inflammatory infiltrate in the gastric mucosa, which is chemoattracted by different cytokines. Interleukin-8 (IL-8) seems to play an important role in the recruitment of circulating neutrophils, and modulation of IL-8 secretion seems to be a strain marker. This study was designed to examine IL-8 concentrations in the gastric mucosa and their relationship with H. pylori phenotype and histologic findings. METHODS: Gastric biopsies were obtained from the antrum and corpus in 106 patients (69 Hp-positive and 37 Hp-negative). IL-8 levels in the gastric mucosa were analyzed by ELISA and Hp phenotype was determined with a western blot test. RESULTS: 75% of H. pylori strains were CagA+ and 54.2% were VacA+. The Houston classification was used for histologic findings. No association between gastric atrophy or intestinal metaplasia and Hp phenotype was found. The highest IL-8 levels were found in CagA+ infected gastric mucosa, but the difference with respect to infection by a VacA+ strain was not statistically significant. IL-8 levels were highest when neutrophils were the predominant cell in the gastric inflammatory infiltrate (p < 0.05). IL-8 levels were higher in patients with atrophic gastritis than in patients with nonatrophic gastritis (p < 0.05). CONCLUSIONS: In patients with H. pylori infection, IL-8 levels are higher than in Hp-negative patients regardless of Hp phenotype. There is an association between IL-8 and a neutrophilic infiltrate. Perpetuation of a chronic infiltrate could lead to more severe lesions such as atrophic gastritis or intestinal metaplasia, as deduced from the IL-8 levels found in these types of lesion.     

Detection of H.pylori DNA in gastric epithelial cells by in situ hybridization

AIM: To investigate the presence of H.pylori DNA within gastric epithelial cells in patients with H.pylori infection and its possible carcinogenic mechanism. METHODS: Total 112 patients, with pathologically confirmed chronic superficial gastritis, chronic atrophic gastritis, intestinal metaplasia, atypical hyperplasia or gastric cancer were studied. Among them, 28 were H.pylori negative and 84 H.pylori positive. H.pylori DNA in gastric epithelial cells was detected by GenPoint catalyzed signal amplification system for in situ hybridization. RESULTS: In the H.pylori positive group, zero out of 24 chronic superficial gastritis (0.0%), four out of 25 precancerous changes (16.0%) and thirteen out of 35 gastric cancers (37.1%) showed H.pylori DNA in the nucleus of gastric epithelial cells, the positive rates of H.pylori DNA in the nucleus of gastric epithelial cells were progressively increased in chronic superficial gastritis, precancerous changes and gastric cancer groups (chi(2)=12.56, P=0.002); One out of 24 chronic superficial gastritis (4.2%), eleven out of 25 precancerous changes (44.0%) and thirteen out of 35 gastric cancers (37.1%) showed H.pylori DNA in the cytoplasm of gastric epithelial cells (chi(2)=10.86, P=0.004). In the H.pylori negative group, only one patient with gastric cancer was found H.pylori DNA in the nucleus of gastric epithelial cells; Only two patients, one patient with precancerous changes and another with gastric cancer, showed H.pylori DNA in the cytoplasm of gastric epithelial cells. Furthermore, H.pylori DNA must have been in the cytoplasm as long as it existed in the nucleus of gastric epithelial cells. CONCLUSION: H.pylori DNA exists both in the nucleus and the cytoplasm of gastric epithelial cells in patients with H.pylori infections. The pathological progression from chronic superficial gastritis, precancerous changes to gastric cancer is associated with higher positive rates of H.pylori DNA presence in the nucleus of gastric epithelial cells.     

Interaction between Helicobacter pylori infection and untreated coeliac disease on gastric histological pattern

OBJECTIVE: Helicobacter pylori infection is the major agent of gastric damage. Coeliac disease may affect the morphology and function of the entire gastrointestinal tract from the stomach to the colon. The aim of this study was to assess the gastric histological pattern in patients with H. pylori and untreated coeliac disease. MATERIAL AND METHODS: We retrospectively enrolled 183 H. pylori-positive patients with (85, group A) and without (98, group B) untreated coeliac disease. The groups were similar for age, gender and smoking habit, and all the patients came from the same geographical area. Histological evaluation of gastric pattern was performed on 4 biopsies (2 in the antrum, 2 in the corpus). Gastric damage was classified according to the modified Sydney System. Diagnosis of H. pylori infection was based on positivity to histology. The chi-square test was used to assess differences between groups. A p-value <0.05 was considered significant. RESULTS: Group A showed a significantly higher prevalence of follicular gastritis than group B (23.5% versus 12.2%, p=0.045). A significantly lower prevalence of atrophic gastritis was observed in group A compared with that in group B (6% versus 22.5%, p=0.002). The prevalence of chronic superficial gastritis, activity degree and intestinal metaplasia was similar between the two groups. CONCLUSIONS: In patients with H. pylori infection, untreated coeliac disease could represent a risk factor for follicular gastritis and is associated with a lower prevalence of atrophic gastritis. The complex interaction between H. pylori and untreated coeliac disease on Th-1/Th-2 balance in the gastric mucosa could explain these results.     

Helicobacter pylori infection and early gastric cancer

BACKGROUND: Helicobacter pylori has recently been associated with an increased risk of gastric cancer. This study aimed to examine the association between H. pylori, histologic chronic gastritis, and intestinal metaplasia in early gastric cancers of different histologic types. STUDY: Seventy-four patients who were surgically diagnosed as having early gastric cancer were included in this study. All tissue specimens were obtained from patients by endoscopic biopsy and were classified histopathologically as intestinal-type early gastric cancer in 55 patients and diffuse-type early gastric cancer in 19 patients. RESULTS: H. pylori infection was found in 67 patients (90.5%) but not found in seven (9.5%). And the prevalence of H. pylori infection with nongastric cancer patients was also high (68.5%). There was no significant difference between the intestinal-type and the diffuse-type early gastric cancer in chronic active gastritis and atrophic chronic gastritis. Intestinal metaplasia was observed more frequently in patients with the intestinal-type than with the diffuse-type early gastric cancer (P = 0.0102). CONCLUSIONS: Infection with H. pylori has an important relationship to both histopathologic types of early gastric cancer.